Stasis dermatitis_1112 Derm Clinic
A 52-year-old man with a history of type 2 diabetes, hypertension, and hyperlipidemia presented with a rash on his bilateral lower extremities. He stated that he often gets edema on his lower extremities, especially after standing for long periods of time. He recently developed pruritic reddish areas that became progressively more indurated and complained of very xerotic skin.
No previous treatments or OTC medications or moisturizers were reported. Physical exam revealed brown to erythematous/violaceous indurated plaques on bilateral lower extremities .
HOW TO TAKE THE POST-TEST: This Clinical Advisor CME activity consists of 3 articles. To obtain credit, you must also read Itchy leg bullae after a trip outdoors and Erythematous, pruritic leg plaques. The post-test will include questions related to all three articles. Click here to obtain CME/CE credit.
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First described in the 1950s,1 stasis dermatitis causes inflammation on the lower extremities in people who have chronic venous insufficiency. Although not all patients with chronic venous insufficiency will develop stasis dermatitis, most will experience episodes of this skin disease.
Stasis dermatitis is a complex and multifactorial condition influenced by many etiologic factors that act together over time. Although there are no direct reports on the prevalence of stasis dermatitis, researchers studying the prevalence of chronic venous insufficiency and venous ulcers have estimated that slightly more than 1% of the world population has the disease.2
Stasis dermatitis tends to be seen in older individuals, and women are affected more than men. The age of onset is usually in the fifth decade of life but may occur earlier if the patient has suffered trauma or thrombosis, which can give rise to venous insufficiency. The disease may be a precursor to such problematic conditions as venous leg ulcers and lipodermatosclerosis.
Chronic venous insufficiency is the most common factor for the onset of stasis dermatitis. Venous hypertension is caused by a malfunction of the one-way valvular system in the deep venous plexus of the legs.
This incompetence causes a backflow of deoxygenated blood into the deep and superficial regions of the legs, which distends the capillaries and damages the capillary permeability barrier. The damage allows plasma fluid and plasma proteins into the tissue, causing edema. Stasis purpura and hemosiderin deposition also occur secondary to erythrocyte extravasation. The combination of these events causes microangiopathy.3
Metabolic exchange and oxygen diffusion ceases when the tissue becomes edematous and the protein (fibrin) becomes deposited around the vessels (i.e., forms a cuff around dermal capillaries). This slow blood flow causes upregulation of L-selectin on neutrophils, vascular intercellular adhesion molecule ICAM-1, and vascular cell adhesion molecule VCAM-1.4,5 These adhesion molecules act as chemoattractants that keep leukocytes (neutrophils and macrophages) alive and active in the perivascular environment. Upregulation causes an increase in neutrophils, which have been reported to be up to 40 times their normal level in those with stasis dermatitis.6
Additionally, pericapillary inflammation is caused by neutrophils releasing inflammatory mediators, free radicals, and proteases. This can trigger focal thrombosis by platelet accumulation in the microvasculature. All of these imbalances in the capillary network will cause fibrosis and tissue remodeling, dysfunction of the lymphatics, and lipoderatosclerosis.2
It is believed that the chronic inflammation and microangiopathy lead to the development of stasis dermatitis. Stasis dermatitis is typically seen in the medial supramalleolar region, which is most susceptible to microangiopathy. The areas of dermatitis occur over dilated varicose veins, and areas that are affected with dermal inflammation may cause hyperproliferation, barrier impairment, and desquamation of the epidermis.
Xerosis is also a common feature. Patients sometimes report severe pruritus, a feeling of heaviness, tingling in the legs, and a burning sensation, which is most likely caused by the release of inflammatory mediators in the dermis and the repeated congestion and decongestion.7 Excoriation at these areas will perpetuate the dermatitis. Such additional factors as contact sensitization and irritant dermatitis due to wound secretion and topical medications may also aggravate the dermatitis.
In the early stages, stasis dermatitis is very mild and may present with xerosis and pruritis of the lower extremities. Due to the chronic venous insufficiency, pitting edema is often appreciated, with greatest severity around the major communicating veins on the shin, calf, and proximal side of the ankle.
As the disease progresses, it may be associated with inflammation and mimic cellulitis. The skin, adipose tissue, and deep fascia become indurated and adhere to each other.7,8 This creates a cuff around the distal calf, giving it the appearance of an inverted champagne bottle.
The skin may also show hemosiderin pigmentation, venous ulcers, and the changes of atrophic blanche (stellate sclerotic areas depleted of capillaries with the formation of peripheral giant capillaries).
In cases of longstanding stasis dermatitis, scaly papules and plaques will develop on the lower legs. By this stage, the affected area is severely pruritic, and oozing and crusting caused by excoriations will be present.
Secondary contact sensitization to components of topical therapies is seen in 58% to 86% of individuals with venous leg ulcers.9 This sensitization will often lead to secondary dissemination that may become generalized and wax and wane for long periods of time.
The stages of stasis dermatitis have different histologic appearances. In acute stasis dermatitis, edema predominates, and large macrovesicles may be seen within the epidermis. Perivascular and superficial lymphocytes are seen in the dermis with occasional exocytosis of lymphocytes into the epidermis.
During the subacute phase, the spongiosis is subtle, and the epidermis begins to thicken and develop parakeratosis. Lymphocytes are still present in the dermis during this stage, but in fewer numbers.
In chronic stasis dermatitis, the thickening of the epidermis is pronounced and often appears psoriasiform.2 The presence of lymphocytes and spongiosis is minimal to nonexistent. All biopsies of stasis dermatitis may reveal such signs of venous hypertension as dilated capillaries surrounded by cuffs of fibrin, hemosiderin deposits, and hyperplastic venules.2,10 During the chronic stages, fibrosis and sclerosis may occur.
Stasis dermatitis is easily diagnosed if signs of venous hypertension are present (e.g., dilated venules, hemosiderin deposits, edema, inverted-champagne-bottle appearance of the calf). Difficulties may arise in differentiating stasis dermatitis from asteatotic eczema, allergic or irritant contact dermatitis, nummular eczema, psoriasis, or mycosis fungoides. Allergic contact dermatitis may be excluded by patch testing. Histologic assessment can differentiate among the other diagnoses.
There are many treatment options for stasis dermatitis; however, the major aim of therapy involves the treatment of such underlying factors as venous hypertension and venous insufficiency. Compression stockings are helpful, but it is important to properly examine peripheral arterial circulation using a Doppler study before starting the treatment in select individuals. Compression of a compromised arterial circulation could cause more problems. Compression therapy uses compression stockings; there are also specialized compression bandages and boots.
In conjunction with compression therapy, such surgical measures as ligation of incompetent communicating veins and removal of insufficient saphenous veins can be taken. Other treatments include topical therapies, particularly corticosteroids and emollients. Topical calcineurin inhibitors are added to individuals with refractory disease.2
Stasis dermatitis is a chronic condition that requires significant life changes to treat effectively. The patient must comply with treatment using leg elevation, compression stockings, and topically applied therapies.
Complications that may arise with stasis dermatitis include nonhealing venous ulcers, increased episodes of allergic contact dermatitis, and lipodermatosclerosis. Ulcers produced by stasis dermatitis should be routinely checked for superinfection. Patient knowledge and education are the most powerful tools available.
The man in this case was treated with compression stockings, leg elevation and triamcinolone 0.1% ointment to be used as needed for pruritus. He was also advised to apply a heavy, bland emollient to the area at least three times a day.
Kerri Robbins, MD, is a resident in the Department of Dermatology at Baylor College of Medicine in Houston.
- Pillsbury DM. The Pathogenesis of Eczema. Proc X Int Congress Dermatol (London, 1952). London: British Medical Association; 1953:58.
- Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology. 3rd ed. St. Louis, Mo.: Elsevier-Mosby; 2012:201-202.
Scharffetter-Kochanek K, Schüller J, Meewes C, et al. [Chronic venous venous ulcus cruris. Pathogenesis and the significance of “aggressive micro-milieus”]. J Dtsch Dermatol Ges. 2003;1:58-67.
- Peschen M, Lahaye T, Hennig B, et al. Expression of the adhesion molecules ICAM-1, VCAM-1, LFA-1 and VLA-4 in the skin is modulated in progressing stages of chronic venous insufficiency. Acta Derm Venereol. 1999;79:27-32.
- Jünger M, Steins A, Hahn M, Häfner HM. Microcirculatory dysfunction in chronic venous insufficiency (CVI). Microcirculation. 2000;7(6 Pt 2):S3-S12.
- Scurr JH, Coleridge-Smith PD. The microcirculation in venous disease. Angiology. 1994;45:537-541.
- Fitzpatrick TB, Johnson RA, Wolff K, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology, 6th ed. New York, N.Y.: McGraw-Hill; 2009:476-477.
- RP Rapini. Practical Dermatopathology. 2nd ed. Philadelphia, Pa.: Elsevier Health Sciences; 2012:45-47.
- Tavadia S, Bianchi J, Dawe RS, et al. Allergic contact dermatitis in venous leg ulcer patients. Contact Dermatitis. 2003;48:261-265.
- Elder DE, Elenitsas R, Johnson BL, et al, eds. Lever’s Histopathology of the Skin. 10th ed. Philadelphia, Pa.: Lippincott Williams & Wilkins; 2009:243.